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AIMS of
STUDY
- Obesity is an independent risk factor for female incontinence in epidemiological
studies1, and has also been implicated in the failure of anti-incontinence surgery2.
It is thought to be a factor in the pathogenesis of genuine stress incontinence
(GSI) in women, although the mechanism is debated. The increased rate of incontinence
may be related to higher abdominal pressure (p.abd) in obese women3. Surprisingly
few data are available on the precise relationship between obesity and p.abd
in women. In morbidly obese patients p.abd correlates well with indices of obesity,
particularly with the sagittal abdominal diameter (SAD)4,5, which is the best
predictor of the volume of intra-abdominal adipose tissue6. The increment in
abdominal pressure on coughing also appears to be related to obesity, with a
significantly smaller increment after massive weight loss in morbidly obese
women5. It has been shown that stress incontinent women have a greater increment
in intravesical pressure on coughing compared to controls, which was considered
important in determining the severity of incontinence, although the relationship
to obesity was not studied7. We therefore investigated in detail the relationship
between obesity and static and dynamic abdominal pressures in a large group
of women of more normal weight.
METHODS
- Women referred for UDS were recruited, height and weight measured, and the
indices height/weight and height/weight2 (i.e. body mass index, or BMI) calculated.
The SAD - i.e. the midline anteroposterior diameter of the abdomen - was measured
at maximal expiration at the umbilicus with the patient supine. P.abd was measured
before UDS in supine, sitting and standing positions using external transducers,
according to ICS guidelines. A subgroup of patients were studied for the pressure
increment during dynamic manoeuvres, recorded at a standard bladder volume of
100 ml. Patients were asked to perform 3 maximal strength coughs, and then to
exhale against different resistances to produce a graded series of Valsalva
manoeuvres.
RESULTS
- 99 women were studied. Weight, BMI and particularly SAD correlated well with
p.abd (p < 0.01 for all correlations). Correlation coefficients for BMI and
SAD in different postures were:
|
|
Supine p.abd |
Sitting p.abd |
Standing p.abd |
|
BMI
(n = 99) |
0.59 |
0.67 |
0.73 |
|
SAD
(n = 90) |
0.62 |
0.69 |
0.79 |
The correlation between indices of obesity and p.abd increased as the patient moved from lying to sitting to standing position. Correlation also increased successively with different indices of obesity in the order: weight < weight/height @ BMI < SAD. Comparing women of normal weight (BMI 20-25, n = 26) with overweight women (BMI 25-30, n = 39), and women with mild obesity (BMI 30-35, n = 18), the mean resting abdominal pressures were 28.9, 32.8 and 40.8 cmH20 respectively. The last 29 recruits were studied in more detail. They were divided into 2 groups according to BMI: group 1: BMI < 28, n =15; and group 2: BMI ³ 28, n =14. The mean maximum increment in pressure on coughing was higher in the more obese women (Group 2: 152 cmH20, Group 1: 127 cmH20), but this difference was not statistically significant. There was no difference in mean pressure increment during maximum valsalva between the groups (Group 1: 29.4 cmH20, group 2 28.0 cmH20).
CONCLUSIONS
- Obesity shows a strong correlation with intra-abdominal pressures. As would
be predicted, the highest correlation is with SAD, and thus with intra-abdominal
obesity. There was a trend towards greater pressure increment on coughing in
more obese women, although this was not statistically significant (possibly
due to the small sample size). GSI in obese women may be partly related to the
fact that the resting abdominal pressure is elevated, and thus lies closer to
the abdominal leak point pressure for the individual. This study also suggests
that the abdominal leak point pressure may be more easily reached in obese women
due to higher pressure increments on coughing, although this requires further
study.
REFERENCES
- 1. World J Urol 1994; 12: 319-22. 2. Br J Obstet Gynaecol 1995; 102: 740-5.
3. J Am Coll Nutr 1988; 7 (2): 147-53. 4. J Int Med 1997; 241: 71-9. 5. Am J
Obstet Gynecol 1992; 167: 392-7. 6. Int J Obes 1991; 15: 19-30. 7. Br J Obstet
Gynecol 1983; 90: 919-33. ACKNOWLEDGEMENT - we would like to thank Lorex Synthélabo
and Southmead Hospital Research Foundation for their financial support for this
study.